Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved activity, selectivity, and safety.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9Y287
UPID:
ITM2B_HUMAN
Alternative names:
Immature BRI2; Protein E25B; Transmembrane protein BRI
Alternative UPACC:
Q9Y287; Q5W0A3; Q96B24; Q9NYH1
Background:
Integral membrane protein 2B (ITM2B), also known as Immature BRI2, Protein E25B, and Transmembrane protein BRI, plays a pivotal role in the processing of amyloid-beta A4 precursor protein (APP), acting as an inhibitor of amyloid-beta peptide aggregation. This protein is crucial in preventing the formation of neurotoxic fibrils, a hallmark of several neurodegenerative disorders.
Therapeutic significance:
ITM2B's involvement in diseases such as Cerebral amyloid angiopathy, ITM2B-related 1 and 2, highlights its potential as a therapeutic target. By modulating ITM2B activity, it may be possible to mitigate amyloid deposition in the brain, offering a promising strategy for treating these debilitating conditions.